Renal cortical necrosis

Introduction Renal cortical necrosis is a rare form of death of kidney tissue that affects only the outer layer (cortex) of some or all of the kidneys without affecting the inner layer (medulla). Renal cortical necrosis can occur at any age. About 10% of cases occur in infants and children. More than half of neonates with renal cortical necrosis have a sudden placental separation (placental dissection) during childbirth; the other most common cause is blood flow bacterial infection (septicemia). In children, renal cortical necrosis can be followed by infection, dehydration, shock or hemolytic uremic syndrome. In adults, bacterial sepsis causes cortical necrosis to account for about one-third of all cases.

Cause

Renal cortical necrosis: a rare form of arterial infarction. It is characterized by cortical tissue necrosis followed by calcification. It is located in the area under the capsule, and is not involved in the near medulla and medulla. Renal cortical necrosis can occur at any age. Among women, complications of pregnancy (such as placental abruption, placenta previa, uterine bleeding, puerperal sepsis, amniotic fluid embolism, intrauterine death, pre-eclampsia) accounted for more than 50% of cases, while bacterial sepsis accounted for 30%. Other causes include hemolytic-uremic syndrome, hyperacute rejection of transplanted kidneys, burns, pancreatitis, snake bites and poisoning (such as phosphorus, arsenic). About 10% of cases occur in infants and children. In neonates, more than 50% of cases are caused by placental abruption, and the second common cause is bacterial sepsis. In children, infection, loss of extracellular capacity, shock and hemolytic-uremic syndrome are common causes. Suspicious mechanisms include vasospasm, activation of coagulation mechanisms, endotoxin, immune damage and direct endothelial cell damage. The damage is very similar to the general Shwartzman phenomenon in animal experiments. Renal cortical necrosis is the result of obstruction of renal cortical arterioles due to various diseases. Other causes include rejection of transplanted kidneys, burns, inflammation of the pancreas (pancreatitis), injury, snake bites, and poisoning. For example, phosphorus and arsenic poisoning.

an examination

Related inspection

Urine inclusion body examination renal angiography

Different forms of cortical necrosis and acute renal failure may be difficult. However, this diagnosis should be considered when there is sudden auria with gross hematuria and hypochondriac pain in any of the above clinical conditions. Fever and leukocytosis are common, even in the absence of sepsis. The urine contains many proteins, red blood cells and white blood cells, red blood cell casts, kidney cell casts and wide tube types. If measured early, serum lactate dehydrogenase and alanine aminotransferase levels are elevated. In the early stages, mild hypertension or even hypotension is common. However, accelerated or malignant hypertension is typical in patients who regain partial residual renal function.

A clear diagnosis shows flaky or diffuse cortical necrosis by biopsy, but renal radiography is useful. The series of radiological angiography initially showed an increase in the kidney, which gradually narrowed down, sometimes reaching about 50% of normal within 6-8 weeks. At this stage, calcification occurs, often linear, at the junction of the cortex and medulla. obvious.

The diagnosis can usually be established by ultrasound or CT scan. Renal biopsy or angiography can also be performed, but most cases do not need to be done. Calcium deposition on the X-ray film suggests renal cortical necrosis. But this happens in the late stages of the disease, the lesions begin to heal, and only 20% to 50% in the patient.

Differential diagnosis

Need to be identified with the following symptoms:

Renal cortical thinning: Chronic glomerulonephritis is the final stage of development of different types of glomerulonephritis. The lesion is characterized by a large number of glomerular glassy changes and sclerosis, also known as chronic sclerosing glomerulonephritis. From the naked eye, the kidneys are reduced in size and the surface is diffuse and fine-grained. The cut cortex is thinned and the boundary of the cortex is unclear. Increased fat around the renal pelvis. The gross lesion of chronic nephritis is called secondary granular pyknosis.

Acute renal failure: the cause of acute renal failure is complicated, and it is a clinical syndrome caused by various factors. There is no perfect classification method for the etiology classification. According to the habit, it is divided into prerenal, renal and post-renal acute renal failure.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.